Spasticity is a prevalent and potentially disabling symptom common in individuals with multiple sclerosis. Adequate evaluation and management of spasticity requires a careful assessment of the patient’s history to determine functional impact of spasticity and potential exacerbating factors, and physical examination to determine the extent of the condition and culpable muscles. A host of options for spasticity management are available: therapeutic exercise, physical modalities, complementary/alternative medicine interventions, oral medications, chemodenervation, and implantation of an intrathecal baclofen pump. Choice of treatment hinges on a combination of the extent of symptoms, patient preference, and availability of services.
Key points
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Spasticity is a prevalent and potentially disabling symptom common in individuals with multiple sclerosis.
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Adequate evaluation and management of spasticity requires a careful assessment of the patient’s history to determine functional impact of spasticity and potential exacerbating factors, and physical examination to determine the extent of the condition and culpable muscles.
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A host of options for spasticity management are available: therapeutic exercise, physical modalities, complementary/alternative medicine interventions, oral medications, chemodenervation, and implantation of an intrathecal baclofen pump.
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Choice of treatment hinges on a combination of the extent of the symptoms, patient preference, and availability of services.
Case study examples
In this discussion of the evaluation and management of spasticity in multiple sclerosis (MS), it will be helpful to begin with two clinical scenarios. The first is an example of a common initial presentation of spasticity. Patient A is a 40-year-old woman with a 7-year history of relapsing remitting MS. Her disease course has been stable since initiation of glatiramer acetate (Copaxone) several years ago. She has no other medical history and is not on other medication besides supplemental vitamins. Functionally she is a very active individual and uses no assistive devices. She presents with tripping and near falls, involving catching her right toe, which occur mostly in the evening or at the end of a long hike. Her goal is to remain active with her outdoor activities. She has never had a spasticity treatment regimen.
The second case is an example of multifactorial spasticity. Patient B is a 50-year-old man with a 20-year history of primary progressive MS. His disease course has been a slow, steady decline and he has never been on a disease-modifying agent. He has multiple medical comorbidities including active coronary artery disease, hypertension, hyperlipidemia, nephrolithiasis, and neurogenic bladder with suprapubic catheter. Functionally he is quadriplegic, but for many years has “used” his lower extremity spasticity to briefly perform standing pivot transfers with assistance, but uses a power wheelchair for all other mobility. Recently he began to have nighttime adductor spasticity with persistent scissoring of his legs that is uncomfortable and is interfering with his sleep. His spasticity treatment regimen for the past 10 years has been baclofen 20 mg at night, diazepam 5 mg at night, positioning, and daily stretching. His goal is to improve comfort and positioning in bed, and minimize side effects of medication.
Case study examples
In this discussion of the evaluation and management of spasticity in multiple sclerosis (MS), it will be helpful to begin with two clinical scenarios. The first is an example of a common initial presentation of spasticity. Patient A is a 40-year-old woman with a 7-year history of relapsing remitting MS. Her disease course has been stable since initiation of glatiramer acetate (Copaxone) several years ago. She has no other medical history and is not on other medication besides supplemental vitamins. Functionally she is a very active individual and uses no assistive devices. She presents with tripping and near falls, involving catching her right toe, which occur mostly in the evening or at the end of a long hike. Her goal is to remain active with her outdoor activities. She has never had a spasticity treatment regimen.
The second case is an example of multifactorial spasticity. Patient B is a 50-year-old man with a 20-year history of primary progressive MS. His disease course has been a slow, steady decline and he has never been on a disease-modifying agent. He has multiple medical comorbidities including active coronary artery disease, hypertension, hyperlipidemia, nephrolithiasis, and neurogenic bladder with suprapubic catheter. Functionally he is quadriplegic, but for many years has “used” his lower extremity spasticity to briefly perform standing pivot transfers with assistance, but uses a power wheelchair for all other mobility. Recently he began to have nighttime adductor spasticity with persistent scissoring of his legs that is uncomfortable and is interfering with his sleep. His spasticity treatment regimen for the past 10 years has been baclofen 20 mg at night, diazepam 5 mg at night, positioning, and daily stretching. His goal is to improve comfort and positioning in bed, and minimize side effects of medication.
Spasticity in multiple sclerosis
Spasticity can manifest in any condition that has upper motor neuron (UMN) lesions, including MS. The prevalence of spasticity in MS can be as high as 80%, and can present clinically and functionally in a variety of ways. Clinically, spasticity can manifest as stiffness of a muscle, muscle cramping, clonus, or periodic muscle spasms (flexor and extensor). It can present as a focal area of muscle tightness in an extremity or as a more diffuse process involving the torso and multiple extremities. Spasticity can be mild and may not interfere with function; however, up to one-third of patients may experience moderate to severe spasticity that limits activities of daily living and is associated with negative implications for quality of life.
Spasticity can be a highly variable symptom that can be worsened by various stimuli. In general, it is worsened by any noxious stimuli to the body, which could be as simple as a change in temperature or body position, or more complex, such as acute illness. Common conditions that may worsen spasticity include infection (most commonly of the urinary tract), wounds, and constipation.
Pathophysiology of spasticity
In the literature, the definition of spasticity is often that given by Lance in 1980, which states: “Spasticity is a motor disorder characterized by a velocity dependent increase in tonic stretch reflexes (“muscle tone”) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex as one component of the upper motor neurone syndrome.” Spasticity can occur whenever there is a lesion in a UMN pathway. The UMN pathways are descending motor tracts that originate in the cortex or brainstem and directly or indirectly influence the excitability of the lower motor neuron or anterior horn cell. These pathways include the corticospinal (pyramidal) tract, medial reticulospinal tract, lateral vestibular tract, and dorsal reticulospinal tract.
Damage to the central nervous system can interrupt the UMN pathways and can cause a constellation of symptoms called the UMN syndrome. The UMN syndrome consists of positive features such as spasticity and spontaneous spasms and negative features such as weakness and decreased fine-motor control, which together impair functional movement. The constellation of symptoms in the UMN syndrome is detailed in Table 1 .
| Negative | Positive |
|---|---|
| Weakness | Flexor/extensor spasms |
| Reduced dexterity | Spasticity |
| Reduced speed of movement | Dystonia |
| Fatigability | Increased tone |
| Slowed movements | Clonus |
| Hyperactive deep tendon reflexes | |
| Babinski sign |
Initial evaluation of the patient with spasticity
History
Initial evaluation of the patient presenting for management of spasticity should include a focused history and physical examination, an evaluation of the patient’s perception of functional limitations arising from spasticity, and the goals of care. This assessment should include a brief but clear history of the patient’s primary neurologic diagnosis; current symptoms and complaints related to spasticity; prior treatments, including medications, therapies, injections, surgeries, or other interventions; and pertinent medical history, including medication history and anticoagulation status. Review of systems should evaluate for signs and symptoms suggesting possible contributory factors, such as infection or noxious stimuli including fever/chills, dysuria, voiding difficulties, skin wounds, constipation, or acute pain.
Physical Examination
Physical examination should include assessment of the joints involved and surrounding joints, and should include passive and active range of motion, strength, sensation, reflexes, and assessment of spasticity. Several tools are available for rating spasticity, the most common of which are the Modified Ashworth Scale (MAS) and Tardieu scale ( Tables 2 and 3 ).
| Score | |
|---|---|
| 0 | No increase in muscle tone |
| 1 | Slight increase in muscle tone, manifested by a catch and release or by minimal resistance at the end range of motion when the part is moved |
| 1+ | Slight increase in muscle tone, manifested by a catch, followed by minimal resistance throughout the remainder (less than half) of the range |
| 2 | More marked increase in muscle tone throughout most of the range, but affected part is easily moved |
| 3 | Considerable increase in muscle tone, passive movement is difficult |
| 4 | Affected part is rigid |
| Velocities | |
| V1 | As slow as possible, slower than the natural drop of the limb segment under gravity |
| V2 | Speed of limb segment falling under gravity |
| V3 | As fast as possible, faster than the rate of the natural drop of the limb segment under gravity |
| Scoring | |
| 0 | No resistance throughout the course of the passive movement |
| 1 | Slight resistance throughout the course of passive movement, no clear catch at a precise angle |
| 2 | Clear catch at a precise angle, interrupting the passive movement, followed by release |
| 3 | Fatigable clonus with less than 10 s when maintaining the pressure and appearing at the precise angle |
| 4 | Unfatigable clonus with more than 10 s when maintaining the pressure and appearing at a precise angle |
| 5 | Joint is immovable |
The provider should observe, when able, the patient’s functional mobility and any affected activities of daily living to gain further information before formalizing a treatment plan. Consideration that some patients use spasticity to enhance functional mobility (stabilizing gait or transfers) must be considered, to avoid inadvertently decreasing function with spasticity treatment. Common functional measures that can be used are outlined in Box 1 .
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Fugl-Meyer
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Arm Activity Measure (ArmA)
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Barthel Index
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Gait speed
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Adductor tone rating scale
Conservative treatment strategies for spasticity management
Nonpharmacologic and noninvasive treatment interventions for spasticity provide primary or adjunctive intervention options to the individual with MS. Although most interventions have not been rigorously studied by randomized control trials, they are low-risk, empower the individual by providing self-management techniques, and are affordable. These interventions may be appropriate options for patients with less severe spasticity or may serve as adjunctive treatment for those with more severe spasticity ( Box 2 ).
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Stretching: passive, active, static splinting, dynamic splinting, serial casting
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Heat
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Ice
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Vibration
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Electrical stimulation
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Extracorporeal shock-wave therapy
Stretching
Stretching is most often the primary conservative recommendation for spasticity management. An effective active or passive range-of-motion program accomplishes 2 aims: to minimize spasticity-inducing quick stretch of tight muscles, and to preserve range of motion and thus avoid contracture, a secondary complication of spasticity. Although limited data are available on the optimal frequency and type of stretching exercises or splints for spasticity management, weight-bearing stretches appear to be superior to non–weight-bearing stretches, particularly for lower extremity spasticity. In addition, prolonged static stretching appears to have a greater effect. In the patient who cannot perform an adequate active stretching program, range of motion may be preserved or improved with serial casting and static or dynamic splinting. Prolonged stretch with casting or splinting may be particularly useful when performed in addition to chemodenervation injections.
Electrical Stimulation
Electrical stimulation has long been recognized for its effects on diminishing spasticity. Stimulation of either antagonists or agonists has been found to produce beneficial effects with reduction of spasticity symptoms. A variety of specific devices have been used for this purpose, including transcutaneous electrical nerve stimulation, functional electrical stimulation, and neuromuscular electrical stimulation. Electrical stimulation also appears to be an effective adjunctive therapy to botulinum toxin injections.
Cryotherapy
For many years, cryotherapy has been known as an effective treatment for spasticity. Cold may be applied in the form of cold baths, cold packs/towels, or vapocoolant sprays. Local application of cryotherapy agents can be applied to agonist or antagonist muscles to treat spasticity. Cold decreases input to the central nervous system by inhibiting sensory afferents; in addition, muscle spindle activity and motor nerve conduction is diminished, resulting in a decrease in spasticity. However, temporary increases in muscle hyperexcitability occur following the application of cryotherapy, which may explain its use in applying treatment to antagonist muscle groups. The effect of icing is short lived, owing to subsequent rewarming of tissues. Cooling may have a general therapeutic effect in patients with MS. In addition, cryotherapy has the benefit of being very accessible and affordable; as Mead and Knott stated eloquently in 1966, “cold is available for the price of ice.”
Heat
Although superficial heat (in the form of hot packs, paraffin, diathermy, or infrared application) and deep heat (as applied by ultrasound) have been studied regarding their use in decreasing pain and spasticity in neurologic disorders, there is little objective evidence for the benefit of heat in the literature. The risks of heat therapy in patients with MS must be considered alongside any benefit, given the possibility of heat sensitivity or exacerbation of neurologic symptoms when using heat in this population. In addition, heat must be used with caution in patients with impaired sensation, owing to the risk of burns or injury.
Vibration
Vibration is another well-known modality used to decrease spasticity. Direct application of vibration to a muscle produces contraction of that muscle, and relaxation of the antagonist muscle. This phenomenon is referred to as the tonic vibration reflex. While local muscle vibration has been the mainstay of this therapy, more recently whole-limb and whole-body vibration has been evaluated in small studies, suggesting improvement in spasticity.
Extracorporeal Shock-Wave Therapy
A few small studies provide evidence of benefit for shock-wave therapy applied to hypertonic muscles. The mechanism of effect of this treatment is unclear, but it has been suggested that extracorporeal shock-wave therapy (ESWT) modifies the characteristics of muscle fibrosis and promotes nitric oxide synthesis. These trials demonstrate significant clinical improvement in spasticity and range of motion following a single treatment of ESWT. The effect of ESWT on spasticity in these studies was found to last for longer than 2 to 3 months. Another recent study compared the additive effect of ESWT with that of electrical stimulation following botulinum toxin injections for spasticity, and found significantly greater improvement in both spasticity and pain in the ESWT group. Of note, ESWT has been evaluated primarily in patients with stroke and cerebral palsy, and not specifically in individuals with MS.
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